• Asian Pacific Journal of Cancer Prevention
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• 제16권6호
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• pp.2161-2166
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• 2015

Estrogen receptors (ERs) are steroid receptors located in the cytoplasm and on the nuclear membrane. The sequence similarities of human $ER{\alpha}$, mouse $ER{\alpha}$, rat $ER{\alpha}$, dog $ER{\alpha}$, and cat $ER{\alpha}$ are above 90%, but structures of $ER{\alpha}$ may different among species. Estrogen can be agonist and antagonist depending on its target organs. This hormone play roles in several diseases including breast cancer. There are variety of the relative binding affinity (RBA) of ER and estrogen species in comparison to $17{\beta}-estradiol$ (E2), which is a natural ligand of both $ER{\alpha}$ and $ER{\beta}$. The RBA of the estrogen species are as following: diethyl stilbestrol (DES) > hexestrol > dienestrol > $17{\beta}-estradiol$ (E2) > 17- estradiol > moxestrol > estriol (E3) >4-OH estradiol > estrone-3-sulfate. Estrogen mimetic drugs, selective estrogen receptor modulators (SERMs), have been used as hormonal therapy for ER positive breast cancer and postmenopausal osteoporosis. In the postgenomic era, in silico models have become effective tools for modern drug discovery. These provide three dimensional structures of many transmembrane receptors and enzymes, which are important targets of de novo drug development. The estimated inhibition constants (Ki) from computational model have been used as a screening procedure before in vitro and in vivo studies.

• Journal of Ginseng Research
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• 제40권3호
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• pp.251-259
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• 2016

Background: Estrogen signaling pathways are modulated by exogenous factors. Panax ginseng exerts multiple activities in biological systems and is classified as an adaptogen. Zearalenol is a potent mycoestrogen that may be present in herbs and crops arising from contamination or endophytic association. The goal of this study was to investigate the impact of P. ginseng, zearalenol and estradiol in tests on spermatozoal function. Methods: The affinity of these compounds for estrogen receptor (ER)-alpha and beta ($ER{\alpha}$ and $ER{\beta}$)-was assessed in receptor binding assays. Functional tests on boar spermatozoa motility, movement and kinematic parameters were conducted using a computer-assisted sperm analyzer. Tests for capacitation, acrosome reaction (AR), and chromatin decondensation in spermatozoa were performed using microscopic analysis. Results: Zearalenol-but not estradiol ($E_2$)- or ginseng-treated spermatozoa-decreased the percentage of overall, progressive, and rapid motile cells. Zearalenol also decreased spontaneous AR and increased chromatin decondensation. Ginseng decreased chromatin decondensation in response to calcium ionophore and decreased AR in response to progesterone ($P_4$) and ionophore. Conclusion: Zearalenol has adverse effects on sperm motility and function by targeting multiple signaling cascades, including $P_4$, $E_2$, and calcium pathways. Ginseng protects against chromatin damage and thus may be beneficial to reproductive fitness.

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2002년도 춘계학술대회(Genomics, Proteomics, and Risk Assesment):환경독성 및 위해성 평가 국제 심포지움
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• pp.75-75
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• 2002

• 한국가축번식학회지
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• 제26권2호
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• pp.183-192
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• 2002

본 연구는 임신 및 분만후 rat에 oxytocin을 투여후 혈장, 자궁 및 태반 조직에서 estradiol-17$\beta$, progesterone, prostaglandin F$_2$$_{\alpha}$ 및 prostaglandin E$_2$그리고 자궁 조직의 oxytocin 수용체의 함량 사이의 관계에 대하여 조사하였다. 임신 rat에 oxytocin 투여 후 혈장 estradiol-17$\beta$의 농도는 임신 말기에 서서히 증가하여 임신 22일에 최고를 기록하였고 분만 후 1일에는 임신 16일 수준으로 감소하였다. Progesterone 농도는 임신 18일부터 분만 후 1일에 유의성 있는(p<0.05) 감소를 보였다. Prostaglandin F$_2$$_{\alpha}$ 및 Prostaglandin E$_2$농도는 임신 14일에서 임신 22일에 공히 상승하여 임신 22일에 최고를 기록하였고 분만 후 1일에는 급격히 감소하였다. Estradiol-17$\beta$의 농도는 자궁 조직에서 임신 14일에서 20일까지 서서히 증가하다가 임신 22일에 급격한 증가를 기록하였고 분만 후 1일에는 급격히 감소하여 임신 14일 수준을 유지하였으며 progesterone 농도는 임신 16일에 상승을 보인 후 임신 20일까지 급격히 감소하였고 분만 후 1일까지 같은 수준을 유지하였다. Prostaglandin F$_2$$_{\alpha}$ 및 prostaglandin E$_2$농도는 자궁조직에서 임신 말기 전기간에 상승하여 임신 22일에 최고를 기록한 후 분만 후 1일에는 급격히 감소하여 임신 14일과 비교하여 70% 수준을 기록하였다. Prostaglandin F$_2$$_{\alpha}$ 농도는 태반 조직에서 임신 14일에서 임신 22일까지 지속적으로 증가하였고 분만 후 1일에는 급격히 감소하였으며 prostaglandin E$_2$의 농도는 임신 14일에서 20일에 증가한 후 분만 후 1일까지 감소하였다. Oxytocin 수용체의 농도는 자궁 조직에서 임신 20일에서 임신 22일 사이에 급격히 증가한 후 분만 후 1일까지 비슷한 수준을 기록하였다. 이상에서와 oxytocin투여에 의한 임신 rat에 있어서 progesterone 농도의 감소에 이은 estradiol-17 $\beta$, prostaglandin F$_2$$_{\alpha}$, prostaglandin E$_2$및 oxytocin 수용체 농도의 증가는 조기에 시작되었다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권11호
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• pp.6761-6767
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• 2013

The nuclear receptor, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$), is expressed in various cancer cells including breast, prostate, colorectal and cervical examples. An endogenous ligand of $PPAR{\gamma}$, 15-deoxy-${\Delta}^{12,14}$ prostaglandin $J_2$ (PGJ2), is emerging as a potent anticancer agent but the exact mechanism has not been fully elucidated, especially in breast cancer. The present study compared the anticancer effects of PGJ2 on estrogen receptor alpha ($ER{\alpha}$)-positive (MCF-7) and $ER{\alpha}$-negative (MDA-MB-231) human breast cancer cells. Based on the reported signalling cross-talk between $ER{\alpha}$ and $ER{\alpha}$, the effect of the $ER{\alpha}$ ligand, $17{\beta}$-estradiol (E2) on the anticancer activities of PGJ2 in both types of cells was also explored. Here we report that PGJ2 inhibited proliferation of both MCF-7 and MDA-MB-231 cells by inducing apoptotic cell death with active involvement of mitochondria. The presence of E2 potentiated PGJ2-induced apoptosis in MCF-7, but not in MDA-MB-231 cells. The $ER{\alpha}$ antagonist, GW9662, failed to block PGJ2-induced activities but potentiated its effects in MCF-7 cells, instead. Interestingly, GW9662 also proved capable of inducing apoptotic cell death. It can be concluded that E2 enhances $ER{\alpha}$-independent anticancer effects of PGJ2 in the presence of its receptor.

• 대한핵의학회지
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• 제12권2호
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• pp.1-5
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• 1978

For clinical application of radioreceptor assay, we studied preliminarily the distribution of estrogen receptor in various organs of rabbit by a dextran-charcoal method using $6,7-^3H-estradiol$. The results were expressed as binding index, which is the ratio of specific estradiol receptor binding radioactivity to total radioactivity. The materials consist of 5 female rabbits and 3 male rabbits. The results were as follows: 1) Female rabbits The binding index was highest in the uterine tissue. This binding index of the uterine tissue was 9.4 times that of the liver, 21.9 times that of the kidney, 24.6 times that of the brain, 28.1 times that of the lung and 65.7 times that of the muscle. 2) Male rabbits The binding index was highest in the liver and decreased in the order of the kidney, the testis, the lung, the brain and the muscle. It is suggested that the estrogen receptor is not confined to any specific target organ but is widely distributed in the various organs, to a different degree.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.23-23
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• 2003

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon (AhR) ligands suppress 17${\beta}$-estradiol (E)-induced responses in the rodent uterus and mammary tumors and in human breast cancer cells. Treatment of ZR-75, T47D and MCF-7 human breast cancer cells with TCDD induces proteasome-dependent degradation of endogenous estrogen receptor ${\alpha}$ (ER${\alpha}$).(omitted)

• 한국수정란이식학회:학술대회논문집
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• 한국수정란이식학회 2002년도 국제심포지엄
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• pp.111-111
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• 2002

Stroke occurs when local thrombosis, embolic particle or the rupture of blood vessele interrupts the blood floe to the brain. $\beta$-estradiol 17-valerate has been reported to exert neuroprotective effects when administered before an ischemic insult. Recently, the pathophysiology of cerebral ischemia has been studied extensively in rat with various methods. In the present study, we investigates whether $\beta$-estrodiol 17-valerate can protect against brain injury. RNA sample were extracted from the hippocampus of female rat, reverse-transcription in the presence of [$\alpha$32p] dATP. Differential gene express-ion profiles were revealed (Bone morphogenetic protein type 1A receptor, Protein disulphide isomerase, Leukemia inhibitor factor receptor, cytochrome bc- 1 complex-x core P, thiol-specific antioxidant protein). RT-PCR was used to validate the relative expression pattern obtained by the cDNA array. The precise relationship between the early expression of recovery genes and stroke is a matter of luther investigation. This Study was supported by the Korea Science and Engineering Foundation(KOSEF) through the Biohealth Products Research Center(BPRC), Inje University, Korea.

• 대한의생명과학회지
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• 제15권3호
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• pp.171-177
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• 2009

This study investigated whether increased adiposity is prevented by estrogen replacement in female ovariectomized (OVX) C57BL/6J mice, an animal model of human menopause and whether these metabolic changes reflect the inhibitory action of estrogen on peroxisome proliferator-activated receptor $\gamma$ ($PPAR{\gamma}$)-regulated gene expression. Treatment of $17{\beta}$-estradiol for the last one week of the experiment decreased high fat diet-induced body weight gain and white adipose tissue mass compared to OVX control mice. Histological analysis showed that administration of $17{\beta}$-estradiol to mice decreased the size of adipocytes in parametrial adipose tissue versus OVX control mice. In addition, $17{\beta}$-estradiol reduced the adipose expression of $PPAR{\gamma}$ as well as $PPAR{\gamma}$ target genes such as adipocyte fatty acid binding protein and tumor necrosis factor $\alpha$. These results suggest that $17{\beta}$-estradiol may inhibit adiposity through reducing the $PPAR{\gamma}$ activities in female OVX mice.

• 대한의생명과학회지
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• 제14권3호
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• pp.131-137
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• 2008

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.